Nonoperative management of acute complicated diverticulitis is highly effective. For patients with free air remote from the site of perforation, nonoperative management is able to convert an emergent situation into an elective one in 93% of cases. The decision to attempt nonoperative therapy must be made based on the patient's physiologic state and associated comorbidities.

HuR is a ubiquitous nucleocytoplasmic RNA binding protein that exerts pleiotropic effects on cell growth and tumorigenesis. In this study, we explored the impact of conditional, tissue-specific genetic deletion of HuR on intestinal growth and tumorigenesis in mice. Mice lacking intestinal expression of HuR (Hur IKO mice) displayed reduced levels of cell proliferation in the small intestine and increased sensitivity to doxorubicin-induced acute intestinal injury, as evidenced by decreased villus height and a compensatory shift in proliferating cells. In the context of ApcMin mice, a transgenic model of intestinal tumorigenesis, intestinal deletion of the HuR gene caused a 3-fold decrease in tumor burden characterized by reduced proliferation, increased apoptosis and decreased expression of transcripts encoding anti-apoptotic HuR target RNAs. Similarly, Hur IKO mice subjected to an inflammatory colon carcinogenesis protocol (AOM-DSS administration) exhibited a 2-fold decrease in tumor burden. Hur IKO mice showed no change in ileal Asbt expression, fecal bile acid excretion or enterohepatic pool size that might explain the phenotype. Moreover, none of the HuR targets identified in Apc Min/+Hur IKO were altered in AOM-DSS treated Hur IKO mice, the latter of which exhibited increased apoptosis of colonic epithelial cells where elevation of a unique set of HuR-targeted pro-apoptotic factors was documented. Taken together, our results promote the concept of epithelial HuR as a contextual modifier of pro-apoptotic gene expression in intestinal cancers, acting independently of bile acid metabolism to promote cancer. In the small intestine, epithelial HuR promotes expression of pro-survival transcripts that support Wnt-dependent tumorigenesis, whereas in the large intestine epithelial HuR indirectly downregulates certain pro-apoptotic RNAs to attenuate colitis-associated cancer.

Inhibition of nuclear factor kappaB activation by IkappaBSR gene transfer improves transplanted lung graft oxygenation, decreases pulmonary edema and neutrophil sequestration, and reduces apoptotic cell death after experimental lung transplantation.

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Obesity is associated with an increased risk of overall and pouch-related complications following IPAA. Obese patients should be counseled preoperatively about these risks accordingly.

Patients with T3N0 colon cancer with inadequate lymph node harvest who receive adjuvant chemotherapy have increased overall survival. Despite this survival benefit, a fraction of these patients receive adjuvant chemotherapy. Barriers to chemotherapy are multifactorial.

Patients undergoing colorectal surgery with an ileostomy return to the hospital after discharge twice as frequently as those with a primary anastomosis or colostomy, often to hospitals other than the primary institution. As postdischarge health-care utilization becomes a measured quality metric, it is increasingly important to help these patients to safely transition to home.

Lung transplantation is the treatment of choice for end-stage pulmonary diseases. A limited donor supply has resulted in 4000 patients on the waiting list. Currently, 10-20% of donor organs offered for transplantation are deemed suitable under the selection criteria, of which 15-25% fail due to primary graft dysfunction (PGD). This has spawned efforts to reexamine the current selection criteria as well as search for alternative donor lungs selection criteria. In this study, we attempt to further our understanding of PGD by observing the changes in gene expression across donor lungs that developed PGD versus those that did not. From our analysis, we have obtained differentially expressed transcripts that were involved in signaling, apoptosis and stress-activated pathways. Results also indicate that metallothionein 3 was over expressed in lungs that didn't develop PGD. This is the first such attempt to perform expression profiling of actual human lungs used for transplantation, for the identification of a molecular signature for PGD.